POS1309 ASSOCIATION BETWEEN RED CELL DISTRIBUTION WIDTH AND INTERSTITIAL LUNG DISEASE IN SYSTEMIC SCLEROSIS
Authors: L. L. Holguín Arias, L. Sorrentino, J. A. Brigante, D. Yucra, R. Gomez, M. D. L. P. Menendez, M. S. Menendez, M. Rivero, A. Benitez, C. Peon, M. J. Gamba, C. Soliz, M. Iudici, A. Hamaui, D. Dubinsky
Journal: Annals of the Rheumatic Diseases (2023)

<h3>Background</h3> Interstitial lung disease (ILD) and pulmonary arterial hypertension (PHT) account for 60% of deaths related to scleroderma (SSc) [1]. The Red Cell Distribution Width (RDW) is a biomarker that has been used as a marker of poor prognosis in various pathologies <sup>[2-9]</sup>. In SSc, the RDW has been found to be elevated in PHT and has been proposed as a predictor of cardiorespiratory compromise <sup>[10-11]</sup>. <h3>Objectives</h3> To evaluate the association between the increase in RDW and the presence of ILD in patients with SSc. <h3>Methods</h3> Observational, retrospective, multicenter, cross-sectional study of patients with SSc (ACR/ EULAR 2013) between 1/1/2011 to 8/31/2021. Other concomitant autoimmune diseases, malignancy, active infections, anemia, recent transfusions, cardiovascular, renal, or hepatic disease were excluded. The diagnosis of ILD was made by high-resolution computed tomography (HRCT) and the extension evaluated by Goh criteria¹². A review of medical records was performed, collecting relevant clinical and demographic characteristics. <h3>Results</h3> Seventy-five patients were included, with a mean age of 59.4 years (SD 14.1, 95% CI 56-63), 67 (89%) were women. A median of 8 years of disease evolution was observed (IQR 8). ILD was observed in 50 (66,6%) patients while 25 (33.3%) did not. According to Leroy's classification, limited SSc (lcSSc) was observed in 50 patients (66,6%) and diffuse SSc (dSSc) in 24 (33,3%); the last classification was significantly associated with the presence of ILD, as was as MRSS (Modified Rodnan Skin Thickness Score)&gt; 14, digital ulcers, and positive ATA (DNA topoisomerase I), unlike ACA (anticentromere antibodies) (Table 1). The most frequent HRCT pattern was NSIP (Nonspecific interstitial pneumonia) in lcSSc (66.6%). An association was found between dSSc and fibrotic patterns (fNSIP and UIP). OR 6, 95% CI 1.6-21 (p 0.009). The extension of the disease was measured in 44 patients (6 missing data), being limited in 25 (57%) and extensive in 19 (43%). The extensive form was correlated with a higher RDW mean (p &lt; 0.0001). The MRSS was measured in 70 patients, being less than 14 in 63 (90%). 100% of the patients with mRSS &gt; 14 had a high RDW (p 0.01). Increased RDW was evidenced in the group with ILD, with a statistically significant difference (OR 6.06 95%CI 2-17 p 0.001). The median RDW in the groups with isolated ILD and ILD plus PHT was significantly higher than in patients without lung disease (p &lt; 0.001). We found no significant difference between the ILD and ILD plus PHT groups (p 0.350) (Figure 1). <h3>Conclusion</h3> We have been able to show that there is a significant relationship between the increase in RDW and the presence of ILD in patients with SSc; this association was more significant for the extensive forms of the disease as well as fibrotic patterns. These findings are relevant as the RDW is an easily accessible parameter that could be used in the follow-up of patients with SSc, and an elevation not explained by other causes of the RDW could be an alarming marker to search more exhaustively for the presence of cardiorespiratory compromise. The limitations of the study are those of any retrospective study, the presence of missing data in addition to the limited number of patients. It is necessary to continue studies with a larger number of patients to grant robustness to the results. <h3>References</h3> [1]Muangchan, et al. The Journal of Rheumatology 2013; 40; 9. [2]Cottin and Brown. Respiratory Research (2019) 20:13 [3]L. A. Allen et al. Journal of Cardiac Failure, vol. 16, no. 3, pp. 230–238, 2010. [4]S. Dabbah et al. American Journal of Cardiology, vol. 105, no. 3, pp. 312–317, 2010. [5]Abul et al. Chronic Respiratory Disease 2014, Vol. 11(2) 73–81 [6]Smukowska-Gorynia A, et al. Heart, Lung and Circulation (2017). [7]Hampole et al. Am J Cardiol 2009;104:868–872 [8]Thayer, T. E. et al. Annals of the American Thoracic Society. doi:10.1513/annalsats.201809-594oc. [9]Jie Yang et al. Canadian Respiratory Journal Volume 2019, Article ID 3853454. [10]Farkas N et al (2014) Rheumatology (Oxford) 53:1439–1445. [11]Forhecz Z et al. Am Heart J 2009;158:659-66. <h3>Acknowledgements:</h3> NIL. <h3>Disclosure of Interests</h3> None Declared.